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Endocrine Mechanism (endocrine + mechanism)
Selected AbstractsEndocrine mechanisms of primate life history trade-offs: Growth and reproductive maturation in vervet monkeysAMERICAN JOURNAL OF HUMAN BIOLOGY, Issue 6 2009Patricia L. Whitten Life history theory predicts that the timing of maturation will result from a trade-off between growth and the age of first reproduction. This trade-off and its mechanisms of action are still poorly understood in many species and have not been well studied at the individual level. This study examined hypothesized trade-offs between growth and reproductive maturation in wild populations of vervet monkeys (Cercopithecus aethiops) from Kenya, East Africa. Individuals were sampled from four populations in widely separated sites differing in temperature, altitude, and rainfall. Biological samples and morphometric measures were collected from 50 adult males, 83 adult females, and 225 juveniles. Gonadal steroids and leptin levels were analyzed by radioimmunoassay of sera from 136 juvenile males and 90 juvenile females. Cross-sectional profiles of morphometric and endocrine data were used to assess the onset and cessation of growth in relation to sexual maturation. Gonadal steroids were used to assess sexual maturation and breeding onset. Leptin was used as an index of nutritional state. Estimates of mortality were derived from population age-structure. Across populations, higher resource productivity and nutrient status were associated with more rapid growth. Shorter growth duration was associated with earlier reproductive onset. These findings provide support for models of trade-offs between the timing of growth completion and reproductive onset, but they are contradicted by the evidence that reproduction precedes the cessation of growth in these populations. The biphasic actions of estradiol provide an alternative model and mechanism for the growth-reproduction trade-off. Am. J. Hum. Biol., 2009. © 2009 Wiley-Liss, Inc. [source] Use of freshwater rotifer Brachionus calyciflorus in screening assay for potential endocrine disruptorsENVIRONMENTAL TOXICOLOGY & CHEMISTRY, Issue 12 2000Benjamin L. Preston Abstract eports of the effectsofendocrinedisruptorsonaquatic invertebrates arebecoming increasingly common. However, little is known about the endocrine systems of most aquatic invertebrates, limiting the development of assays based on endocrine mechanisms. As a result, endocrine disruption is often inferred through the effects caused by the chemical of interest, making it difficult to rule out other mechanisms of toxicity. To be a good candidate for an endocrine disruptor, effects should be observed in processes known to be under endocrine control, at life stages where endocrine signals are known to be active, and at concentrations below acute and chronic toxic effects. We developed a 96-h reproductive assay using the freshwater rotifer Brachionus calyciflorus to screen for potential endocrine disruptors and examined cadmium, chlorpyrifos, naphthol, pentachlorophenol, estradiol, methoprene, precocene, nonylphenol, flutamide, and testosterone for effects on asexual and sexual reproduction. Flutamide, testosterone, and nonylphenol inhibited fertilization of sexual females at concentrations of 1, 10, and 50 ,g/L, respectively. The fertilization no-observable-effect concentrations (NOECs) for these compounds were 5 to 200 times lower than previously described reproduction NOECs for B. calyciflorus. Sexual reproduction was inhibited with no effects on asexual reproduction, increasing the likelihood that these specific reproductive effects occurred through an endocrine mechanism. Rotifer reproduction assays may be a useful, rapid, and inexpensive method for screening compounds suspected to have endocrine disrupting activity in aquatic invertebrates. [source] Development and evolution of adaptive polyphenismsEVOLUTION AND DEVELOPMENT, Issue 1 2003H. Frederik Nijhout SUMMARY Phenotypic plasticity is the primitive character state for most if not all traits. Insofar as developmental and physiological processes obey the laws of chemistry and physics, they will be sensitive to such environmental variables as temperature, nutrient supply, ionic environment, and the availability of various macro- and micronutrients. Depending on the effect this phenotypic plasticity has on fitness, evolution may proceed to select either for mechanisms that buffer or canalize the phenotype against relevant environmental variation or for a modified plastic response in which some ranges of the phenotypic variation are adaptive to particular environments. Phenotypic plasticity can be continuous, in which case it is called a reaction norm, or discontinuous, in which case it is called a polyphenism. Although the morphological discontinuity of some polyphenisms is produced by discrete developmental switches, most polyphenisms are due to discontinuities in the environment that induce only portions of what is in reality a continuous reaction norm. In insect polyphenisms, the environmental variable that induces the alternative phenotype is a token stimulus that serves as a predictor of, but is not itself, the environment to which the polyphenism is an adaptation. In all cases studied so far, the environmental stimulus alters the endocrine mechanism of metamorphosis by altering either the pattern of hormone secretion or the pattern of hormone sensitivity in different tissues. Such changes in the patterns of endocrine interactions result in the execution of alternative developmental pathways. The spatial and temporal compartmentalization of endocrine interactions has produced a developmental mechanism that enables substantial localized changes in morphology that remain well integrated into the structure and function of the organism. [source] Thyroid hormone and reproduction: Regulation of estrogen receptors in goldfish gonadsMOLECULAR REPRODUCTION & DEVELOPMENT, Issue 9 2010Erik R. Nelson Abstract There is increasing evidence that thyroid hormones influence reproduction in vertebrates. However, little information is available on the mechanisms by which this happens. As a first step in determining these mechanisms, we test the hypothesis that the estrogen receptor subtypes (ER,, ER,-1, and ER,-2) are regulated by the thyroid hormone, (T3), in the gonads of goldfish. All three subtypes were down-regulated by T3 in the testis or ovary. We also found evidence that T3 decreased pituitary gonadotropin expression and decreased transcript for gonadal aromatase. Collectively, it appears that T3 acts to diminish estrogen signaling by (1) decreasing pituitary LH expression and thus steroidogenesis, (2) down-regulating gonadal aromatase expression and thus decreasing estrogen synthesis from androgens, and (3) decreasing sensitivity to estrogen by down-regulating the ER subtypes. Goldfish are seasonal breeders, spawning once a year, and thus have two distinct periods of growth: somatic and reproductive. Circulating thyroid hormone levels have been found to increase just after spawning. Therefore, we propose that this may be an endocrine mechanism that goldfish use to switch their energy expenditure from reproductive to growth efforts in the goldfish. Mol. Reprod. Dev. 77: 784,794, 2010. © 2010 Wiley-Liss, Inc. [source] Dietary Fructose: Implications for Dysregulation of Energy Homeostasis and Lipid/Carbohydrate MetabolismNUTRITION REVIEWS, Issue 5 2005Peter J. Havel DVM Fructose intake and the prevalence of obesity have both increased over the past two to three decades. Compared with glucose, the hepatic metabolism of fructose favors lipogenesis, which may contribute to hyperlipidemia and obesity. Fructose does not increase insulin and leptin or suppress ghrelin, which suggests an endocrine mechanism by which it induces a positive energy balance. This review examines the available data on the effects of dietary fructose on energy homeostasis and lipid/carbohydrate metabolism. Recent publications, studies in human subjects, and areas in which additional research is needed are emphasized. [source] Use of freshwater rotifer Brachionus calyciflorus in screening assay for potential endocrine disruptorsENVIRONMENTAL TOXICOLOGY & CHEMISTRY, Issue 12 2000Benjamin L. Preston Abstract eports of the effectsofendocrinedisruptorsonaquatic invertebrates arebecoming increasingly common. However, little is known about the endocrine systems of most aquatic invertebrates, limiting the development of assays based on endocrine mechanisms. As a result, endocrine disruption is often inferred through the effects caused by the chemical of interest, making it difficult to rule out other mechanisms of toxicity. To be a good candidate for an endocrine disruptor, effects should be observed in processes known to be under endocrine control, at life stages where endocrine signals are known to be active, and at concentrations below acute and chronic toxic effects. We developed a 96-h reproductive assay using the freshwater rotifer Brachionus calyciflorus to screen for potential endocrine disruptors and examined cadmium, chlorpyrifos, naphthol, pentachlorophenol, estradiol, methoprene, precocene, nonylphenol, flutamide, and testosterone for effects on asexual and sexual reproduction. Flutamide, testosterone, and nonylphenol inhibited fertilization of sexual females at concentrations of 1, 10, and 50 ,g/L, respectively. The fertilization no-observable-effect concentrations (NOECs) for these compounds were 5 to 200 times lower than previously described reproduction NOECs for B. calyciflorus. Sexual reproduction was inhibited with no effects on asexual reproduction, increasing the likelihood that these specific reproductive effects occurred through an endocrine mechanism. Rotifer reproduction assays may be a useful, rapid, and inexpensive method for screening compounds suspected to have endocrine disrupting activity in aquatic invertebrates. [source] Profound changes in the GH,IGF-I system in adolescent girls with IDDM: can IGFBP1 be used to reflect overall glucose regulation?PEDIATRIC DIABETES, Issue 3 2000MU Halldin Disturbances in the relations between insulin, growth hormone (GH) and insulin-like growth factor I (IGF-I) may be a major cause behind deteriorated metabolic control in adolescent girls with type I diabetes. These patients have increased GH secretion and low IGF-I concentrations. The aim of this study was to identify possible endocrine mechanisms behind good and poor glycaemic control in such girls, focusing on the insulin,GH,IGF-I axis. Ten girls with well-controlled insulin-dependent diabetes mellitus (IDDM), hemoglobin A1c (HbA1c) 6.5±0.4% (normal range 3.9,5.2%) and nine healthy controls were investigated and compared with 11 girls with poor glucose regulation, HbA1c 10.9±0.4%, and their corresponding controls. Serum profiles of glucose, insulin, GH and IGF-binding protein 1 (IGFBP1) were analysed in addition to IGF-I and HbA1c. Two interesting observations were made. GH concentrations were equally elevated in the two diabetic groups regardless of metabolic control (mean 24 h GH , girls with poorly controlled diabetes 10.0±1.0 mU/L vs 9.8±1.7 , girls with well-controlled diabetes; p=ns). Likewise, the IGF-I concentrations were reduced to the same extent (233±19 vs 242±23 ,g/L; p=0.75). Secondly, despite similar insulin concentrations (mean 24 h insulin , girls with poorly controlled diabetes 22.9±2.6 and girls with well-controlled diabetes 27.3±2.9 mU/L, respectively; p=0.26), there was a marked difference in IGFBP1 concentrations between the two groups with IDDM (mean IGFBP1 , girls with poorly controlled diabetes 70.5±9.1 ,g/L vs girls with well-controlled diabetes 28.6±3.3; p<0.001). Despite equally elevated GH concentrations that may induce insulin resistance, the markedly lower concentrations of IGFBP1 in the well-controlled group indicate a higher hepatic insulin sensitivity in these girls compared with those with a poor control. Furthermore, in spite of similar total IGF-I concentrations, the lower IGFBP1 concentrations may result in higher IGF-I bioactivity in the well-controlled group. This may be reflected in better growth of the well-controlled group whose height of 168.7±0.9 vs 163.6±1.2 cm was significantly different (p<0.004). IGFBP1 may be a marker of overall insulinization in adolescents with type 1 diabetes, independent of the absolute insulin dose used for therapy. [source] Regulation of uterine function by cytokines in cows: Possible actions of tumor necrosis factor-,, interleukin-1, and interferon-,ANIMAL SCIENCE JOURNAL, Issue 3 2006Kiyoshi OKUDA ABSTRACT When animals do not become pregnant, regression of the corpus luteum (CL) is essential for normal cyclicity because it allows the development of a new ovulatory follicle. Luteal regression is caused by a pulsatile release of prostaglandin (PG) F2, from the uterus in the late luteal phase in most mammals including cattle. Although it has been proposed in ruminants that pulsatile PGF2, secretion is generated by a positive feedback loop between luteal and/or hypophyseal oxytocin and uterine PGF2,, the bovine endometrium may possess other mechanisms for initiation of luteolytic PGF2, secretion. There is increasing evidence that several cytokines mainly produced by immune cells modulate CL and uterine function in many species. Tumor necrosis factor-, (TNF-,) stimulates PGF2, output from bovine endometrium not only at the follicular phase but also at the late luteal phase. Administration of TNF-, at a high concentration prolongs luteal lifespan, whereas administration of a low concentration of TNF-, accelerates luteal regression in cows. The data obtained from the authors' previous in vitro and in vivo studies strongly suggest that TNF-, is a crucial factor in regulating luteolysis in cows. The authors' recent study has shown that interleukin-1, mediates PG secretion from bovine endometrium as a local regulator. Furthermore, interferon-, (IFN-,) suppresses the action of TNF-, on PGF2, synthesis by the bovine endometrium in vitro, suggesting that IFN-, plays a luteoprotective role by inhibiting TNF-,-induced PGF2, production in early pregnancy. The purpose of the present review is to summarize current understanding of the endocrine mechanisms that regulate uterine function by cytokines during the estrous cycle and early pregnancy in cows. [source] The role of oxytocin in parturitionBJOG : AN INTERNATIONAL JOURNAL OF OBSTETRICS & GYNAECOLOGY, Issue 2003Andrew M. Blanks Oxytocin and the oxytocin receptor have two important roles in labour. Evidence in all mammalian species suggests that neurohypophysical oxytocin plays a role in the expulsive phase and, although there are less supporting data, a role for oxytocin in the initiation of labour is likely. The initiation of labour may be mediated in women and rhesus monkeys by paracrine rather than endocrine mechanisms. Although initial characterisation of the oxytocin knockout mouse suggested that oxytocin is not important in this species, subsequent investigations have demonstrated that oxytocin is important for the precise timing of the onset of labour. Studies in knockout mice also confirm important interrelationships between oxytocin and prostaglandins. Oxytocin stimulates prostaglandin release in many species, mainly in the decidua/uterine epithelium. The effects of oxytocin are mediated by tissue-specific oxytocin receptor expression, which leads directly to contraction in the myometrium and prostaglandin formation in the decidua. There is a dramatic increase in oxytocin receptor expression in these tissues in late pregnancy and pharmacological inhibition delays delivery, which suggests that, in contrast to oxytocin, the oxytocin receptor is essential for normal labour. [source] | |||||||||||||